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Pericardial Disease


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Pericardial Disease

  1. 1. Pericardial Diseases Piti Niyomsirivanich, MD. Reference : Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.
  2. 2. ANATOMY AND PHYSIOLOGY OF THE PERICARDIUM <ul><li>The pericardium is composed of two layers </li></ul><ul><ul><li>the visceral pericardium </li></ul></ul><ul><ul><ul><li>single layer of mesothelial cells adherent to the epicardial surface of the heart </li></ul></ul></ul><ul><ul><li>the fibrous parietal layer </li></ul></ul><ul><ul><ul><li>about 2 mm thick in normal humans and surrounds most of the heart. </li></ul></ul></ul><ul><ul><ul><li>acellular and contains both collagen and elastin fibers. </li></ul></ul></ul><ul><ul><ul><li>Collagen  low levels of stretch </li></ul></ul></ul>
  3. 3. <ul><li>The pericardial space or sac is contained within these two layers and normally contains up to 50 ml of serous fluid . </li></ul><ul><li>The parietal pericardium has ligamentous attachments to the diaphragm, sternum , and other structures in the anterior mediastinum. </li></ul><ul><li>The only noncardiovascular macrostructures associated with the pericardium are the phrenic nerves , which are enveloped by the parietal pericardium. </li></ul>
  4. 5. <ul><li>the normal pericardium does have functions </li></ul><ul><ul><li>it maintains the position of the heart relatively constant. </li></ul></ul><ul><ul><li>function as a barrier to infection and provides lubrication between visceral and parietal layers. </li></ul></ul><ul><li>The pericardium is well innervated with mechanoreceptors and chemoreceptors and phrenic afferents. </li></ul><ul><ul><li>reflexes arising from the pericardium and/or epicardium (e.g., the Bezold-Jarisch reflex), as well as transmission of pericardial pain . </li></ul></ul>
  5. 6. <ul><li>its restraining effect on cardiac volume. </li></ul><ul><ul><li>At low applied stresses  it is elastic </li></ul></ul><ul><ul><li>As stretch increases  stiff </li></ul></ul>
  6. 7. <ul><ul><li>The contact pressure is proportionally more important for the right heart , whose filling pressures are normally lower than the left heart. </li></ul></ul>
  7. 8. THE PASSIVE ROLE OF THE NORMAL PERICARDIUM IN HEART DISEASE <ul><li>When the cardiac chambers dilate rapidly, </li></ul><ul><ul><li>the restraining effect can become markedly augmented </li></ul></ul><ul><ul><li>resulting in a hemodynamic picture </li></ul></ul><ul><ul><ul><li>resembling both cardiac tamponade and constrictive pericarditis </li></ul></ul></ul><ul><ul><li>The most common example is acute RV myocardial infarction (MI), </li></ul></ul><ul><ul><li>the right heart dilates markedly and rapidly </li></ul></ul><ul><ul><li>total heart volume > pericardial reserve volume. </li></ul></ul><ul><ul><li>increased pericardial constraint </li></ul></ul><ul><ul><li>paradoxical pulse ,Kussmaul sign </li></ul></ul>
  8. 9. <ul><li>Chronic cardiac dilation (e.g., caused by dilated cardiomyopathy or regurgitant valvular disease) </li></ul><ul><ul><li>the pericardium undergoes chronic adaptation to accommodate marked increases in cardiac volume. </li></ul></ul>
  10. 11. <ul><li>defined as symptoms and/or signs resulting from pericardial inflammation of no more than 1 to 2 weeks' duration . </li></ul><ul><li>can occur in a wide variety of these diseases (denoted by asterisks), but the majority of cases are idiopathic . </li></ul>
  11. 12. Categories of Pericardial Disease and Selected Specific Etiologies <ul><li>Idiopathic    </li></ul><ul><li>Infectious    </li></ul><ul><ul><li>Viral (echovirus, coxsackievirus, adenovirus, cytomegalovirus, hepatitis B, infectious mononucleosis, HIV/AIDs)    Bacterial ( Pneumococcus, Staphylococcus, Streptococcus, mycoplasma, Lyme disease, Haemophilus influenzae, Neisseria meningitidis, and others)    Mycobacteria (Mycobacterium tuberculosis, Mycobacterium avium-intracellulare)    Fungal (histoplasmosis, coccidiomycosis)    Protozoal    </li></ul></ul><ul><li>Immune-inflammatory    </li></ul><ul><ul><li>Connective tissue disease [*] (systemic lupus erythematosus, rheumatoid arthritis, scleroderma, mixed)    Arteritis (polyarteritis nodosa, temporal arteritis)    Inflammatory bowel disease    Early post–myocardial infarction    Late post–myocardial infarction (Dressler syndrome), [*] late postcardiotomy/thoracotomy, [*] late posttrauma [*] Drug induced [*] (e.g., procainamide, hydralazine, isoniazid, cyclosporine)    Neoplastic disease    Primary: mesothelioma, fibrosarcoma, lipoma, and so on    Secondary [*] : breast and lung carcinoma, lymphomas, Kaposi sarcoma </li></ul></ul>
  12. 13. Categories of Pericardial Disease and Selected Specific Etiologies <ul><li>Radiation induced [*] Early postcardiac surgery    Hemopericardium    Trauma    Post–myocardial infarction free wall rupture    Device and procedure related: percutaneous coronary procedures, implantable defibrillators, pacemakers, post–arrhythmia ablation, post–atrial septal defect closure, post–valve repair/replacement    Dissecting aortic aneurysm    Trauma    Blunt and penetrating, [*] post–cardiopulmonary resuscitation [*]    Congenital    Cysts, congenital absence    Miscellaneous    </li></ul><ul><ul><li>Cholesterol (“gold paint” pericarditis)    Chronic renal failure, dialysis related    Chylopericardium    Hypothyroidism and hyperthyroidism    Amyloidosis    Aortic dissection </li></ul></ul>
  13. 14. <ul><li>The incidence is difficult to quantify </li></ul><ul><ul><li>> there are undoubtedly many undiagnosed cases . </li></ul></ul><ul><li>At autopsy, the frequency is approximately 1 percent . </li></ul><ul><li>Pericarditis is relatively common in patients presenting to the ER </li></ul><ul><ul><li>> 5 % of nonischemic chest pain </li></ul></ul><ul><ul><li>1% of cases with ST elevation. </li></ul></ul>
  14. 15. History and Differential Diagnosis <ul><li>almost always presents with chest pain . </li></ul><ul><li>A few cases are diagnosed during evaluation of associated symptoms </li></ul><ul><ul><li>such as dyspnea or fever </li></ul></ul><ul><ul><li>incidentally in noncardiac manifestations of systemic diseases </li></ul></ul><ul><ul><ul><li>such as rheumatoid arthritis or systemic lupus erythematosus (SLE). </li></ul></ul></ul>
  15. 16. <ul><li>The pain of pericarditis can be severe. It is variable in quality but often sharp and almost always pleuritic . </li></ul><ul><li>Pericardial pain typically has a relatively rapid onset and sometimes begins remarkably abruptly. </li></ul><ul><ul><li>It is most commonly substernal, but can also be centered in the left anterior chest or epigastrium. </li></ul></ul><ul><ul><li>Left arm radiation is not unusual. </li></ul></ul>
  16. 17. <ul><li>radiation to trapezius ridge, which is highly specific for pericarditis . </li></ul><ul><li>Pericardial pain is almost always relieved by sitting forward and worsened by lying down. </li></ul><ul><li>Associated symptoms </li></ul><ul><ul><li>dyspnea, cough, and occasionally hiccoughs. </li></ul></ul><ul><li>A history of cancer or an autoimmune disorder, high fevers with shaking chills, skin rash, or weight loss should alert the physician to specific diseases that can cause pericarditis. </li></ul>
  17. 18. <ul><li>Diagnoses most easily confused with pericarditis include </li></ul><ul><ul><li>pneumonia or pneumonitis with pleurisy (which may coexist with pericarditis), pulmonary embolus/infarction, costochondritis, and gastroesophageal reflux disease. </li></ul></ul><ul><li>Acute pericarditis is usually relatively easily distinguished from myocardial ischemia/infarction on clinical and other grounds, but coronary angiography is occasionally required to resolve this issue. </li></ul><ul><li>Other considerations include </li></ul><ul><ul><li>aortic dissection, intraabdominal processes, pneumothorax, and herpes zoster pain (before skin lesions appear.) </li></ul></ul><ul><ul><li>Finally, acute pericarditis is occasionally the presenting manifestation of a preceding, clinically silent MI. </li></ul></ul>
  18. 19. Physical Examination <ul><li>Patients with uncomplicated acute pericarditis often appear uncomfortable and anxious and may have low-grade fever and s inus tachycardia . </li></ul><ul><li>Otherwise, the only abnormal physical finding is the friction rub caused by contact between visceral and parietal pericardium. </li></ul><ul><li>The classic rub is pathognomonic of pericarditis. </li></ul><ul><li>It consists of three components corresponding to ventricular systole, early diastolic filling, and atrial contraction and is similar to the sound made when walking on crunchy snow. </li></ul>
  19. 20. <ul><li>The rub is usually loudest at the lower left sternal border , often extends to the cardiac apex , and is best heard with the patient leaning forward . </li></ul><ul><li>It is often dynamic , disappearing and returning over short periods of time. </li></ul><ul><li>Sometimes what is considered a pericardial rub has only two or even one component. </li></ul>
  20. 21. Laboratory Testing <ul><li>Electrocardiogram </li></ul><ul><ul><li>The electrocardiogram (ECG) is the most important laboratory test for diagnosing acute pericarditis. </li></ul></ul><ul><ul><li>The ST segment vector typically points leftward , anterior and inferior , with ST segment elevation in all leads except AVR and often V1. </li></ul></ul><ul><ul><li>Thus the term “diffuse” is a slight misnomer. </li></ul></ul><ul><ul><li>Usually, the ST segment is coved upward and resembles the current of injury of acute, transmural ischemia. </li></ul></ul>
  21. 22. <ul><li>In other cases the ST segment more closely resembles early repolarization. </li></ul><ul><li>PR segment depression is also common </li></ul><ul><ul><li>PR depression can occur in the absence of ST elevation </li></ul></ul><ul><ul><li>and be the initial ECG manifestation of acute pericarditis </li></ul></ul>
  22. 23. <ul><li>ECG abnormalities other than ST elevation and PR depression are unusual in patients presenting soon after the onset of symptoms of acute pericarditis. </li></ul><ul><li>Subsequent ECG changes are quite variable. </li></ul>
  23. 24. <ul><li>In others, the elevated ST segment passes through the isoelectric point </li></ul><ul><ul><li>and progresses to ST segment depression and T wave inversions in leads with upright QRS complexes. </li></ul></ul><ul><ul><li>The latter changes can persist for weeks and months. </li></ul></ul><ul><li>these ECG changes can be difficult to distinguish from myocardial ischemia. </li></ul>
  24. 25. <ul><li>ECG abnormalities other than the above should be considered carefully </li></ul><ul><ul><li>As examples, AV block  Lyme disease, </li></ul></ul><ul><ul><li>pathological Q  silent MI with pericardial pain as its first manifestation, </li></ul></ul><ul><ul><li>low voltage or electrical alternans point toward significant effusion. </li></ul></ul>
  25. 26. <ul><li>Modest elevations of the white blood cell count , typically 11,000 to 13,000 ml with a mild lymphocytos is, are common in acute idiopathic pericarditis. </li></ul><ul><li>Higher counts are an alert for the presence of other etiologies. </li></ul><ul><li>The erythrocyte sedimentation rate (ESR) should be no more than modestly elevated in acute idiopathic pericarditis. </li></ul><ul><li>Unusually high values may be a clue to etiologies such as autoimmune diseases or tuberculosis. </li></ul>
  26. 27. Cardiac Enzymes and Troponin Measurements <ul><li>Surprisingly large numbers of patients with a diagnosis of </li></ul><ul><ul><li>acute pericarditis without other evidence of myocarditis or MI have elevated creatine kinase MB fraction and/or troponin I values </li></ul></ul><ul><li>Pericarditis patients with elevated biomarkers of myocardial injury almost always have ST segment elevation. </li></ul><ul><li>elevations of troponin I without creatine kinase </li></ul><ul><ul><li> adjacent epicardial inflammation rather than a true myocarditis </li></ul></ul>
  27. 28. Chest Radiograph <ul><li>CXR is usually normal in uncomplicated acute idiopathic pericarditis. </li></ul><ul><li>Occasionally, small pulmonary infiltrates or pleural effusions are present, </li></ul><ul><li>bacterial pericarditis often occurs in conjunction with severe pneumonia . </li></ul><ul><li>Mass lesions and enlarged lymph nodes suggestive of neoplastic disease also have great significance. </li></ul>
  28. 29. <ul><li>Tuberculous pericarditis can occur with or without associated pulmonary infiltrates. </li></ul><ul><li>Pulmonary vascular congestion may signal coexistent, severe myocarditis. </li></ul>
  29. 30. Echocardiography <ul><li>The echocardiogram is normal in most patients with acute idiopathic pericarditis. </li></ul><ul><li>The main reason for its performance is to exclude an otherwise silent effusion . </li></ul><ul><li>Moderate or larger effusions are unusual </li></ul>
  30. 31. Natural History and Management <ul><li>keep in mind that controlled data are limited . </li></ul><ul><li>Initial management should be focused on screening for specific etiologies </li></ul><ul><ul><li>In young women  test for SLE. </li></ul></ul>
  31. 32. <ul><li>Acute idiopathic pericarditis is a self-limited disease without significant complications or recurrence In 70 to 90 percent of patients. </li></ul><ul><li>If laboratory data support the clinical diagnosis, symptomatic treatment with nonsteroidal antiinflammatory drugs (NSAIDs) should be initiated </li></ul><ul><li>Because of its excellent safety profile, we prefer ibuprofen (600 to 800 mg po three times daily) with discontinuation if pain is no longer present after 2 weeks . </li></ul>
  32. 33. <ul><li>Many patients have gratifying responses to the first dose or two of an NSAID , and most respond fully and need no additional treatment. </li></ul><ul><li>Reliable patients with no more than small effusions who respond well to NSAIDs need not be admitted to a hospital . </li></ul>
  33. 34. <ul><li>Patients who do not respond well initially , have larger effusions, or suspicion of an etiology other than idiopathic pericarditis should be hospitalized for additional observation, diagnostic testing, and treatment as needed. </li></ul>
  34. 35. <ul><li>Patients who respond slowly or inadequately to NSAIDs may require supplementary narcotic analgesics to allow time for a full response and/or a brief course of colchicine or prednisone . </li></ul><ul><li>Colchicine is administered as a 2 to 3 mg oral loading dose followed by 1 mg daily for 10 to 14 days . </li></ul><ul><li>Prednisone 60 mg by mouth is administered daily for 2 days with tapering to zero over a week . </li></ul>
  35. 36. <ul><li>Perhaps 15 to 30 percent of patients with acute, apparently idiopathic pericarditis who respond satisfactorily to treatment as outlined earlier suffer a relapse after completion of initial therapy </li></ul><ul><li>A pericardial biopsy to look for a specific etiology in patients with recurrent pain without effusion is rarely indicated </li></ul>
  36. 37. <ul><li>Treatment of recurrent pain is empirical. </li></ul><ul><li>For an initial relapse, a second 2-week course of a NSAID is often effective. </li></ul><ul><li>we favor colchicine prophylaxis . Substantial experience has accumulated using chronic colchicine as prophylaxis for recurrent pericardial pain including that caused by idiopathic pericarditis and other etiologies (postthoracotomy, SLE). </li></ul><ul><li>As earlier, the usual dose is a 2- to 3-mg oral load followed by 1 mg by mouth daily. </li></ul><ul><li>Nonsteroidal immunosuppressive therapy with drugs such as azathioprine and cyclophosphamide … experience is extremely limited </li></ul>
  38. 39. Etiology <ul><ul><li>Idiopathic pericarditis and any infection, neoplasm, autoimmune, or inflammatory process (including postradiation and drug induced) that can cause pericarditis can cause an effusion </li></ul></ul><ul><ul><li>high incidence of progression to tamponade are bacterial (including mycobacteria), fungal , and human immunodeficiency virus (HIV)-associated infections and neoplastic involvement. </li></ul></ul>
  39. 40. Pathophysiology and Hemodynamics <ul><li>Formation of an effusion is a component of the response to inflammation when there is an inflammatory and/or infectious process affecting the pericardium. </li></ul><ul><li>pericardial tumor implants </li></ul><ul><li>Lymphomas  by obstructing pericardial lymph drainage. </li></ul><ul><li>effusions in situations with no obvious inflammation (e.g., uremia) is poorly understood. </li></ul>
  40. 41. <ul><li>Cardiac tamponade is characterized by a continuum from an effusion causing minimally detectable effects to full-blown circulatory collapse. </li></ul><ul><li>Determinants of the hemodynamic consequences of pericardial effusion are the level of pressure in the pericardial sac and the ability of the heart to compensate for elevated pressure. </li></ul>
  41. 42. <ul><li>Large, slowly accumulating effusions are often well tolerated , presumably because of chronic changes in the pericardial pressure-volume relation. </li></ul><ul><li>The compensatory response to a significant pericardial effusion includes </li></ul><ul><ul><li>increased adrenergic stimulation and parasympathetic withdrawal , which cause tachycardia and increased contractility. </li></ul></ul><ul><li>those receiving beta-adrenergic blocking drugs are more susceptible to the effects of a pericardial effusion. </li></ul>
  42. 43. <ul><li>As fluid accumulates in the pericardial sac, </li></ul><ul><ul><li>Lt-Rt A and V diastolic pressures rise </li></ul></ul><ul><ul><li>severe tamponade pressure in the pericardial sac, typically 15 to 20 mm Hg </li></ul></ul><ul><li>cardiac volumes progressively decline. </li></ul><ul><li>The decreased preload mainly accounts for the small stroke volume. </li></ul>
  43. 44. <ul><li>two other hemodynamic abnormalities are characteristic of tamponade. </li></ul><ul><ul><li>One is loss of the y descent of the right atrial or systemic venous pressure </li></ul></ul><ul><ul><li>The second characteristic hemodynamic finding is the paradoxical pulse </li></ul></ul><ul><ul><ul><li>large decline in systemic arterial pressure during inspiration (usually defined as a >10 mm Hg drop in systolic pressure) </li></ul></ul></ul><ul><ul><li>Also seen in </li></ul></ul><ul><ul><ul><li>constrictive pericarditis, pulmonary embolus, and pulmonary disease with large variation in intrathoracic pressure. </li></ul></ul></ul>
  44. 46. Low Pressure Temponade <ul><li>Low pressure tamponade occurs when there is a decrease in blood volume in the setting of a preexisting effusion that would not otherwise be significant. </li></ul><ul><li>diuretics are administered to patients with effusions </li></ul><ul><li>Low pressure tamponade is observed during hemodialysis </li></ul>
  45. 47. Regional tamponade <ul><li>sometimes encountered after cardiac surgery </li></ul><ul><ul><li>should be suspected whenever hemodynamic abnormalities exist in a setting in which a regional or loculated effusion is present. </li></ul></ul><ul><ul><li>Large pleural effusions can also compress the heart </li></ul></ul>
  46. 48. Clinical Presentation <ul><li>Asymptomatic unless tamponade is present. </li></ul><ul><li>Patients with tamponade may complain of true dyspnea , the mechanism of which is uncertain because no pulmonary congestion occurs. </li></ul>
  47. 49. <ul><li>In pericardial effusion without tamponade </li></ul><ul><ul><li>the cardiovascular examination is normal except that if the effusion is large , the cardiac impulse may be difficult or impossible to palpate and the heart sounds muffled . </li></ul></ul><ul><ul><li>Tubular breath sounds may be heard in the left axilla or left base because of bronchial compression. </li></ul></ul><ul><ul><li>Beck's triad of hypotension, muffled heart sounds, and elevated jugular venous pressure remains a useful clue to the presence of severe tamponade </li></ul></ul>
  48. 50. <ul><li>Patients with tamponade are almost always uncomfortable, with signs reflecting varying degrees of reduced cardiac output and shock including tachypnea; diaphoresis; cool extremities; peripheral cyanosis; depressed sensorium; and, rarely, yawning. </li></ul><ul><li>hypotension is usually present , although in early stages compensatory mechanisms maintain the blood pressure. </li></ul>
  49. 51. reduced voltage and electrical alternans Low voltage : emphysema, infiltrative myocardial disease, and pneumothorax
  50. 52. Chest Radiograph <ul><li>The cardiac silhouette remains normal until pericardial effusions are at least moderate in size. </li></ul><ul><li>With moderate and larger effusions , the anteroposterior cardiac silhouette assumes a rounded, flasklike appearance . </li></ul><ul><li>Lateral views may reveal the pericardial fat pad sign , a linear lucency between the chest wall and the anterior surface of the heart representing separation of parietal pericardial fat from epicardium. </li></ul>
  51. 53. Echocardiography <ul><li>A pericardial effusion appears as a lucent separation between parietal and visceral pericardium. </li></ul><ul><li>With a true effusion, separation is present for the entire cardiac cycle . </li></ul><ul><li>Small effusions are first evident over the posterobasal left ventricle. </li></ul>
  52. 54. <ul><li>Early diastolic collapse of the right ventricle and collapse of the right atrium (which occurs during ventricular diastole) are sensitive and specific signs </li></ul><ul><li>Right atrial collapse is considered more sensitive . </li></ul><ul><li>RV collapse more specific for tamponade </li></ul>
  53. 55. <ul><li>Distention of the caval vessels that does not diminish with inspiration is also a useful sign </li></ul><ul><li>Doppler velocity recordings demonstrate exaggerated respiratory variation in right- and left-sided venous and valvular flow, </li></ul>
  54. 57. Other Imaging Modalities <ul><li>Computed tomography (CT) and magnetic resonance imaging (MRI) are useful adjuncts to echocardiography in the characterization of effusion and tamponade </li></ul><ul><li>Neither is ordinarily required and/or advisable in sick patients </li></ul><ul><li>Attenuation similar to water suggests transudative, greater than water malignant, bloody or purulent, and less than water chylous effusion. </li></ul>
  55. 58. Management of Pericardial Effusion and Tamponade <ul><li>suspected bacterial or tuberculous pericarditis, bleeding into the pericardial space </li></ul>
  56. 59. Effusions Without Actual or Threatened Tamponade <ul><li>In many cases of effusion when tamponade is neither present nor threatened, a cause will be evident or suggested on the basis of the history (e.g., known neoplastic or autoimmune disease, radiation therapy) and/or previously obtained diagnostic tests. </li></ul><ul><li>When a diagnosis is not clear , an assessment of specific etiologies of pericardial disease should be undertaken. </li></ul><ul><li>TB ,autoimmune diseases and infections (e.g., Lyme disease) and hypothyroidism should be considered </li></ul><ul><li>Serial titers of antibodies to viruses are usually not helpful </li></ul>
  57. 60. <ul><li>In obvious cases </li></ul><ul><li>In occasional situations where pericardiocentesis is necessary for diagnostic purposes, consideration should be given to open drainage with biopsy . </li></ul><ul><li>Occasional patients with large, asymptomatic effusions and no evidence of tamponade. </li></ul><ul><ul><li>The effusions are by definition chronic . </li></ul></ul><ul><li>They are in general stable, and specific etiologies usually do not emerge over time . </li></ul><ul><li>there is a rationale for closed pericardiocentesis following routine evaluation for specific etiologies </li></ul><ul><li>Before undertaking pericardiocentesis , a course of a NSAID or colchicine should be considered . </li></ul>
  58. 61. Effusions with Actual or Threatened Tamponade <ul><li>These patients should be considered as having a true or potential medical emergency. </li></ul><ul><li>Most patients require pericardiocentesis to treat or prevent tamponade. </li></ul><ul><li>idiopathic pericarditis , mild tamponade can be treated with a course of a NSAID and/or colchicine and monitored in the hope that their effusions will shrink rapidly. </li></ul><ul><li>Patients with autoimmune diseases can be treated in the same way and/or with a course of corticosteroids </li></ul>
  59. 62. <ul><li>in whom a decision is made to defer pericardiocentesis </li></ul><ul><ul><li>Hemodynamic monitoring with a pulmonary artery balloon catheter is often useful </li></ul></ul><ul><li>Once actual or threatened tamponade is diagnosed, intravenous hydration should be instituted </li></ul><ul><li>intravenous positive inotropes (dobutamine, dopamine) can be employed but are of limited efficacy </li></ul><ul><li>Hydration and positive inotropes are temporizing measures and should not be allowed to substitute for or delay pericardiocentesis </li></ul>
  60. 63. <ul><li>closed pericardiocentesis is the initial treatment of choice </li></ul>
  61. 64. <ul><li>subxiphoid needle insertion performed under echocardiographic guidance </li></ul><ul><li>Once the needle has entered the pericardial space, a modest amount of fluid should be removed (perhaps 50 to 150 ml) in an effort to produce some degree of hemodynamic improvement. </li></ul><ul><li>Then a guidewire should be inserted </li></ul><ul><li>the needle replaced with a pigtail catheter . </li></ul><ul><li>The catheter can be manipulated with continuing echocardiographic guidance to maximize the amount of fluid removed </li></ul><ul><li>If echocardiographic guidance is unavailable, the needle should be directed toward the right shoulder and then replaced with a catheter for subsequent fluid removal </li></ul>
  62. 65. <ul><li>If a pulmonary artery catheter has been inserted into the right heart, </li></ul><ul><ul><li>pulmonary capillary wedge and systemic arterial pressures and cardiac output should be monitored before, during, and after the procedure. </li></ul></ul><ul><li>Following pericardiocentesis, repeat echocardiography and in many cases continued hemodynamic monitoring are useful to assess fluid reaccumulation . </li></ul>
  63. 66. Analysis of Pericardial Fluid <ul><li>The fluid has the features of a plasma ultrafiltrate. </li></ul><ul><li>analysis of pericardial fluid does not usually have a high yield in identifying the etiology </li></ul><ul><li>routine pericardial fluid measurements should include specific gravity, white blood cell count and differential, hematocrit, and protein content </li></ul><ul><li>Blood in pericardial fluid is nonspecific </li></ul><ul><li>Chylous effusions can occur after traumatic or surgical injury to the thoracic duct or obstruction by a neoplastic process. </li></ul><ul><li>Cholesterol rich (“ gold paint ”) effusions occur in severe hypothyroidism . </li></ul>
  64. 67. <ul><li>Pericardial fluid should be routinely stained and cultured for detection of bacteria, including tuberculosis, and fungi. </li></ul><ul><li>As much fluid as possible should be submitted for detection of malignant cells </li></ul><ul><li>adenosine deaminase (ADA), interferon-gamma, and polymerase chain reaction (PCR </li></ul><ul><ul><li>we believe that a relatively rapid test for tuberculosis (ADA, PCR) should be routine because of the general difficulty of diagnosing tuberculous pericarditis </li></ul></ul>
  65. 68. Pericardioscopy and Percutaneous Biopsy <ul><li>Some experts advocate the routine use of pericardioscopic-guided biopsy in patients with pericardial effusion who do not have an etiologic diagnosis. </li></ul><ul><ul><li>fluoroscopy-guided parietal pericardial biopsy </li></ul></ul><ul><ul><li>extended sampling (18 to 20 samples). </li></ul></ul>
  67. 70. Etiology <ul><li>The pathophysiological consequence of pericardial scarring is markedly restricted filling of the heart </li></ul><ul><li>results in elevation and equilibration of filling pressures in all chambers and the systemic and pulmonary veins. </li></ul><ul><li>almost all ventricular filling occurs early in diastole </li></ul><ul><li>Systemic venous congestion results in hepatic congestion, peripheral edema, ascites, and sometimes anasarca and cardiac cirrhosis. </li></ul>
  68. 71. <ul><li>Failure of transmission of intrathoracic pressure changes during respiration to the cardiac chambers </li></ul>Septal bounce
  69. 72. Clinical Presentation <ul><li>usual presentation consists of signs and symptoms of predominantly right heart failure . </li></ul><ul><ul><li>include lower extremity edema, vague abdominal complaints, and some degree of passive hepatic congestion </li></ul></ul><ul><ul><li>As the disease becomes more severe, hepatic congestion worsens and can progress to ascites and/or anasarca, as well as jaundice caused by cardiac cirrhosis. </li></ul></ul>
  70. 73. Physical Examination <ul><li>markedly elevated jugular venous pressure with a prominent, rapidly collapsing y descent combined with a normally prominent x descent </li></ul><ul><li>W , M </li></ul><ul><li>AF </li></ul><ul><ul><li>the x descent is lost, prominent y descent </li></ul></ul><ul><ul><li>The latter is difficult to distinguish from tricuspid regurgitation </li></ul></ul><ul><li>Kussmaul sign, an inspiratory increase in systemic venous pressure, is usually present </li></ul>
  71. 74. <ul><li>A paradoxical pulse occurs in perhaps one third of patients with constrictive pericarditis </li></ul><ul><li>pericardial knock, an early diastolic sound best heard at the left sternal border and/or the cardiac apex. </li></ul><ul><ul><li>corresponds to the early, abrupt cessation of ventricular filling </li></ul></ul><ul><li>Widening of second heart sound splitting may also be present </li></ul><ul><li>Other signs of chronic hepatic congestion include jaundice, spider angiomata, and palmar erythema. Lower extremity edema is usually present, and anasarca </li></ul>
  72. 75. Electrocardiogram <ul><li>Nonspecific T wave abnormalities are often observed, as well as reduced voltage . Left atrial abnormality may also be present. </li></ul>
  73. 76. Chest Radiograph <ul><li>Pericardial calcification is seen in a minority of patients and should raise the suspicion of tuberculous pericarditis </li></ul>
  74. 77. Echocardiogram <ul><li>pericardial thickening , abrupt displacement of the interventricular septum during early diastole </li></ul><ul><li>signs of systemic venous congestion </li></ul><ul><li>Doppler flow velocity measurements reveal exaggerated respiratory variation </li></ul><ul><ul><li>help distinguish restrictive cardiomyopathy from constrictive pericarditis </li></ul></ul>
  75. 78. Cardiac Catheterization and Angiography <ul><li>assists in discriminating between constrictive pericarditis and restrictive cardiomyopathy </li></ul><ul><li>Right and left heart pressures should be recorded simultaneously </li></ul>
  76. 79. Computed Tomography and Magnetic Resonance Imaging <ul><li>detecting even minute amounts of pericardial calcification & Thickness </li></ul><ul><li>normal pericardium measured by CT is less than 2 mm. </li></ul><ul><li>MRI sensitivity > CT </li></ul>
  77. 80. Differentiating Constrictive Pericarditis from Restrictive Cardiomyopathy
  78. 81. Management <ul><li>Constrictive pericarditis is a progressive disease. </li></ul><ul><li>surgical pericardiectomy is the only definitive treatment & should not be delayed once the diagnosis is made. </li></ul><ul><li>may respond to a course of corticosteroids </li></ul><ul><li>diuretics and salt restriction </li></ul><ul><li>beta-adrenergic blockers and calcium antagonists that slow the heart rate should be avoided </li></ul><ul><ul><li>sinus tachycardia is a compensatory mechanism, </li></ul></ul>
  79. 82. Pericardiectomy <ul><li>performed through either a median sternotomy or a left fifth interspace thoracotomy </li></ul><ul><li>radical excision of as much of the parietal pericardium as possible </li></ul><ul><li>The visceral pericardium is then inspect </li></ul><ul><li>Resection should be considered if it is involved in the disease process. </li></ul><ul><li>Pericardiectomy has a 5 to 15 percent perioperative mortality in patients with constrictive pericarditis </li></ul>
  80. 83. Prognosis <ul><li>From 70 to 80 percent of patients remain free from adverse cardiovascular outcomes at 5 years, </li></ul><ul><li>and 40 to 50 percent at 10 years after pericardiectomy . </li></ul><ul><li>Long-term results are worst in patients with </li></ul><ul><ul><li>radiation-induced disease, impaired renal function, relatively high pulmonary artery systolic pressure, reduced LV ejection fraction, low serum sodium, and advanced age </li></ul></ul>
  82. 85. Viral Pericarditis <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>most common form of pericardial infection </li></ul></ul><ul><ul><li>caused by either direct damage resulting from viral replication or immune responses . </li></ul></ul><ul><ul><li>Echo and Coxsackie viruses are the most common </li></ul></ul><ul><ul><li>Cytomegalovirus has a predilection for immunocompromised patients </li></ul></ul><ul><ul><li>most definitive way to diagnose viral pericarditis is detection of DNA by PCR or in situ hybridization in pericardial fluid </li></ul></ul>
  83. 86. Viral Pericarditis <ul><li>Clinical Features and Management </li></ul><ul><ul><li>In patients with chronic, confirmed viral pericarditis, several immune-mediated treatments are under investigation </li></ul></ul><ul><ul><li>none have been shown to be effective to date . </li></ul></ul>
  84. 87. Bacterial Pericarditis <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>characterized by a purulent effusion </li></ul></ul><ul><ul><li>Direct extension from pneumonia or empyema </li></ul></ul><ul><ul><li>most common agents are staphylococci , pneumococci, and streptococci . </li></ul></ul><ul><ul><li>Hematogenous spread during bacteremia and contiguous spread after thoracic surgery </li></ul></ul>
  85. 88. Bacterial Pericarditis <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>Anaerobic organisms </li></ul></ul><ul><ul><li>can also result from rupture of perivalvular abscesses into the pericardial space </li></ul></ul><ul><ul><li>Rarely , pericardial invasion spreads along facial planes from the oral cavity </li></ul></ul><ul><ul><li>Neisseria can evoke a sterile effusion accompanied by systemic reactions such as arthritis, pleuritis, and ophthalmitis. </li></ul></ul><ul><ul><li>This does not require antibiotic therapy and responds to antiinflammatory drugs. </li></ul></ul>
  86. 89. <ul><li>Clinical Features </li></ul><ul><ul><li>usually high-grade fever with shaking chills and tachycardia </li></ul></ul><ul><ul><li>A pericardial friction rub is present in the majority. </li></ul></ul><ul><ul><li>can take a fulminant course with rapid development of tamponade </li></ul></ul><ul><ul><li>Laboratory findings include </li></ul></ul><ul><ul><ul><li>leukocytosis with marked left shift. </li></ul></ul></ul><ul><ul><ul><li>Pericardial fluid shows polymorphonuclear leukocytosis, low glucose, high protein, and elevated lactate dehydrogenase levels . </li></ul></ul></ul>
  87. 90. <ul><ul><li>chest radiograph shows widening of the cardiac silhouette if the effusion is large </li></ul></ul><ul><li>With gas-producing organisms a lucent air fluid interface may be observed. </li></ul><ul><li>The ECG shows typical ST segment and T wave changes of acute pericarditis , , along with low voltage </li></ul><ul><li>Echocardiography almost always demonstrates a significant pericardial effusion with or without adhesions </li></ul><ul><li>Cardiac tamponade is common and can be confused with septic shock. </li></ul>
  88. 91. <ul><li>Management </li></ul><ul><ul><li>proven bacterial pericarditis should be considered a medical emergency </li></ul></ul><ul><ul><li>prompt closed pericardiocentesis or surgical drainage performed. </li></ul></ul><ul><ul><li>Gram stained and cultured for aerobic and anaerobic bacteria </li></ul></ul><ul><ul><li>Fungal and tuberculosis staining and cultures should also be performed. </li></ul></ul>
  89. 92. <ul><li>Purulent pericardial effusions are likely to recur. Thus surgical drainage with construction of a window is often necessary </li></ul><ul><li>Intrapericardial streptokinase has been administered to selected patients with purulent and/or loculated effusions and may obviate the need for a window </li></ul><ul><li>The prognosis of bacterial pericarditis is generally poor , with survival in the range of 30 percent even in modern series. </li></ul>
  90. 93. Pericardial Disease and Human Immunodeficiency Virus <ul><li>Pericardial disease is the most common cardiac manifestation of HIV </li></ul><ul><ul><li>the most common abnormality is an effusion </li></ul></ul><ul><ul><li>Most are small; asymptomatic </li></ul></ul><ul><ul><li>related to enhanced cytokine </li></ul></ul><ul><ul><li>Congestive heart failure, Kaposi sarcoma, tuberculosis, and other pulmonary infections are independently associated with moderate to large effusions, </li></ul></ul>
  91. 94. <ul><li>In some cases the HIV virus itself appears to be the etiology. </li></ul><ul><li>Tuberculosis is the most common etiology of pericardial effusion in African HIV patients . </li></ul><ul><li>Constrictive pericarditis is rare . When present it is usually secondary to Mycobacterium tuberculosis </li></ul>
  92. 95. <ul><li>Clinical Features </li></ul><ul><ul><li>Symptomatic patients with pericardial disease usually present with dyspnea or chest pain </li></ul></ul><ul><ul><li>The most common infectious agents identified in symptomatic effusions are M. tuberculosis and Mycobacterium avium-intracellulare . </li></ul></ul><ul><ul><ul><li>Cryptococcus neoformans, cytomegalovirus, and Mycobacterium kansasii </li></ul></ul></ul><ul><ul><li>Lymphomas and Kaposi sarcoma are the most common neoplasms associated with effusion </li></ul></ul>
  93. 96. <ul><li>Management </li></ul><ul><ul><li>Asymptomatic patients with small to moderate pericardial effusions do not require treatment . </li></ul></ul><ul><ul><li>Most are idiopathic and usually remain asymptomatic or resolve spontaneously . </li></ul></ul><ul><ul><li>Symptomatic, large effusions should be drained </li></ul></ul>
  94. 97. Tuberculous Pericarditis <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>patients with pulmonary tuberculosis, 1 to 8 percent develop pericardial involvement. </li></ul></ul><ul><ul><li>7 percent of patients who developed cardiac tamponade . </li></ul></ul>
  95. 98. <ul><li>Clinical Features </li></ul><ul><ul><li>subacute to chronic, with fever, malaise, and dyspnea in association with a pericardial effusion </li></ul></ul><ul><ul><li>Cough, night sweats, orthopnea, weight loss, and ankle edema are also common </li></ul></ul><ul><ul><li>The most frequent findings are radiographic cardiomegaly, pericardial rub, fever, and tachycardia </li></ul></ul><ul><ul><li>Findings related to large effusions, paradoxical pulse , hepatomegaly, increased venous pressure , pleural effusion, and distant heart sounds are common </li></ul></ul>
  96. 99. <ul><li>A definitive diagnosis is made by isolating the organism from pericardial fluid or biopsy. </li></ul><ul><li>the yield for isolation from pericardial fluid is low . </li></ul><ul><li>probability of making a diagnosis is increased if both pericardial fluid and biopsy specimens are examined </li></ul><ul><li>a definite role for pericardial biopsy . Pericardial tissue reveals either granulomas or organisms in 80 to 90 percent of cases </li></ul>
  97. 100. <ul><li>Granulomas can be found in rheumatoid and sarcoid pericardial disease. </li></ul><ul><li>Measurement of adenosine deaminase (ADA) was the first modern test to markedly improve the accuracy and speed of diagnosis of tuberculous pericarditis </li></ul><ul><li>ADA greater than 40 units/liter in pericardial fluid has a sensitivity and specificity greater than 90 percent. </li></ul><ul><li>Increased interferon-gamma in pericardial fluid is an additional marker </li></ul>
  98. 101. <ul><li>Management </li></ul><ul><ul><li>The goals of therapy are to treat symptoms , as well as tamponade </li></ul></ul><ul><ul><li>Multidrug antimycobacterial treatment is mandatory </li></ul></ul><ul><ul><li>Corticosteroids did not influence the risk of death or progression to constriction but did speed the resolution of symptoms and decrease reaccumulation of fluid. </li></ul></ul><ul><ul><li>The outcomes suggested that patients who undergo open drainage are less likely to require repeat pericardiocentesis , and there was a trend in the open drainage group toward reduced development of constriction. </li></ul></ul>
  99. 102. <ul><li>If corticosteroids are administered, high doses (1 to 2 mg/kg/day with tapering over 6 to 8 weeks) </li></ul>
  100. 103. Uremic Pericarditis and Dialysis-Associated Pericardial Disease <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>Its pathophysiology has never been fully elucidated , </li></ul></ul><ul><ul><li>but it is correlated with blood levels of blood urea nitrogen (BUN) and creatinine. </li></ul></ul><ul><ul><li>The acute or subacute phase is characterized by shaggy, hemorrhagic, fibrinous exudates on both parietal and visceral surfaces with minimal inflammatory cellular reaction. </li></ul></ul><ul><ul><li>Dialysis-associated pericardial disease is now much more common than classic uremic pericarditis. </li></ul></ul><ul><ul><li>It is characterized by de novo appearance of pericardial disease in patients undergoing chronic dialysis , </li></ul></ul>
  101. 104. <ul><li>Clinical Features </li></ul><ul><ul><li>acute pericarditis with chest pain, fever, leukocytosis, and pericardial friction rub . </li></ul></ul><ul><ul><li>Small, asymptomatic effusions are common </li></ul></ul><ul><ul><li>Alternatively, patients can present with a pericardial effusion causing hypotension during or after ultrafiltration ( low-pressure tamponade ). </li></ul></ul>
  102. 105. <ul><li>Management </li></ul><ul><ul><li>intensive hemodialysis and drainage in patients with effusions . </li></ul></ul><ul><ul><li>Pericardial effusions without hemodynamic compromise usually resolve after several weeks of intensive hemodialysis . </li></ul></ul><ul><ul><li>Treatment of pericardial disease appearing de novo in patients on chronic dialysis is empirical </li></ul></ul><ul><ul><li>Use of NSAIDs for pericardial pain is reasonable , but corticosteroids are probably ineffective . </li></ul></ul><ul><ul><li>A pericardial window may be required and is usually the most effective approach in patients with recurring effusions . </li></ul></ul>
  103. 106. Early Post–Myocardial Infarction Pericarditis and Dressler Syndrome <ul><li>Etiology and Pathophysiology </li></ul><ul><ul><li>occurs during the first 1 to 3 days </li></ul></ul><ul><ul><li>caused by transmural necrosis with inflammation </li></ul></ul><ul><ul><li>40 percent of patients with large, Q-wave MIs have pericardial inflammation </li></ul></ul><ul><ul><li>Thrombolysis and mechanical revascularization appear to have reduced the incidence of this form of pericarditis by at least 50 percent. </li></ul></ul><ul><ul><li>Late pericarditis </li></ul></ul><ul><ul><ul><li>described by Dressler and had an estimated incidence of 3 to 4 percent of MI patients </li></ul></ul></ul><ul><ul><ul><li>Dressler syndrome is believed to have an autoimmune etiology caused by sensitization to myocardial cells </li></ul></ul></ul>
  104. 107. <ul><li>Clinical Features </li></ul><ul><ul><li>early post-MI pericarditis is asymptomatic and identified by auscultation of a rub </li></ul></ul><ul><ul><li>usually within 1 to 3 days after presentation. </li></ul></ul><ul><ul><li>Many are monophasic (usually systolic) and can be confused with murmurs of mitral regurgitation or ventricular septal defect . </li></ul></ul><ul><ul><li>Acute post-MI pericarditis virtually never causes tamponade (except LV free wall rupture) </li></ul></ul><ul><ul><li>An atypical T-wave evolution consisting of persistent upright T waves or early normalization of inverted T waves has also been described and appears to be highly sensitive for early post-MI pericarditis . </li></ul></ul>
  105. 108. <ul><li>Dressler syndrome occurs as early as 1 week to a few months after acute MI . </li></ul><ul><li>Symptoms include fever and pleuritic chest pain . The physical examination may reveal pleural and/or pericardial friction rubs. </li></ul><ul><li>The chest radiograph may show a pleural effusion and/or enlargement of the cardiac silhouette , and the </li></ul><ul><li>ECG often demonstrates ST elevation and T wave changes typical of acute pericarditis . </li></ul>
  106. 109. <ul><li>Management </li></ul><ul><ul><li>Treatment is entirely symptomatic. Augmentation of the usual low-dose aspirin administered to MI patients ( 650 mg three to four times per day for 2 to 5 days ) </li></ul></ul><ul><ul><li>Corticosteroids and perhaps some non-aspirin NSAIDs interfere with conversion of an MI into a scar </li></ul></ul><ul><ul><li>Dressler syndrome is a self-limited disorder , admission to hospital for observation and monitoring should be considered if there is a substantial pericardial effusion </li></ul></ul><ul><ul><li>Aspirin or other NSAIDs are effective for symptomatic relief. </li></ul></ul><ul><ul><li>Colchicine is also likely effective. </li></ul></ul><ul><ul><li>A short course of prednisone , 40 to 60 mg per day with a 7- to 10-day taper, can be used in patients </li></ul></ul>